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Endocrine Abstracts (2016) 41 EP997 | DOI: 10.1530/endoabs.41.EP997

Medical University of Silesia, School of Medicine with the Division of Dentistry, Chair and Department of Histology and Embryology, Zabrze, Poland.


Introduction: Thyroid goiter may be present in different thyroid pathologies, such as non-toxic nodular goiter (NTNG) or Hashimoto’s thyroiditis (HT), as a result of focal hyperplasia of thyrocytes (nodal goiter) or generalized enlargement of thyroid (diffuse goiter). Previous studies have demonstrated that programmed cell death, known as apoptosis, plays an important role in the pathogenesis of many thyroid diseases, especially inflammatory conditions.

Materials and methods: Pathological tissues of 49 patients with thyroid goiter: 38 cases with non-toxic nodular goiter and 11 patients with Hashimoto’s thyroiditis were examined during the study. In a standard immunohistochemical procedure, monoclonal antibodies anti-CD95/Fas and anti-CD253/TRAIL were applied. The number of positively stained cells were counted and expressed as a mean value of at least 10 high power fields (HPF, 400x).

Results: Hashimoto’s thyroiditis demonstrated higher expression of CD95/Fas and CD253/TRAIL in comparison with non-toxic nodular goiter and healthy thyroid gland. Positive staining for CD95/Fas was observed in 100% of HT (2.9 cells/HPF), whereas only 53% of NTNG showed immunoreactivity (1.6 cells/HPF). 91% of HT revealed expression of CD253/TRAIL (4.2 cells/HPF). Only 32% of NTNG demonstrated the presence of CD253/TRAIL (1.9 cells/HPF).

Conclusions: Apoptotic markers could become indicators of disease activity and immunological phenotype. Alterations in the process of apoptosis are implicated in the pathogenesis of autoimmune thyroid diseases, such as Hashimoto’s thyroiditis.

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